Abstract Although many studies regarding ischemic brain damage in the gerbil have been reported, studies on neuronal damage according to various durations of ischemia–reperfusion (I–R) have been ...limited. In this study, we examined neuronal damage/death and glial changes in the somatosensory cortex 4 days after 5, 10 and 15 min of transient cerebral ischemia using the gerbil. To examine neuronal damage, we used Fluoro-Jade B (F-J B, a marker for neuronal degeneration) histofluorescence staining as well as cresyl violet (CV) staining and neuronal nuclei (NeuN, neuronal marker) immunohistochemistry. In the somatosensory cortex, some CV and NeuN positive (+ ) neurons were slightly decreased only in layers III and VI in the 5 min ischemia-group, and the number of CV+ and NeuN+ neurons were decreased with longer ischemic time. The F-J B histofluorescence staining showed a clear neuronal damage in layers III and VI, and the number of F-J B+ neurons was increased with time of ischemia–reperfusion: in the 15 min ischemia-group, the number of F-J B+ neurons was much higher in layer III than in layer VI. In addition, we immunohistochemically examined gliosis of astrocytes and microglia using anti-glial fibrillary acidic protein (GFAP) and anti-ionized calcium-binding adapter molecule 1 (Iba-1) antibody, respectively. In the 5 min ischemia-group, GFAP+ astrocytes and Iba-1+ microglia were distinctively increased in number, and their immunoreactivity was stronger than that in the sham-group. In the 10 and 15 min ischemia-groups, numbers of GFAP+ and Iba-1+ glial cells were much more increased with time of ischemia–reperfusion; in the 15 min ischemia-group, their distribution patterns of GFAP+ and Iba-1+ glial cells were similar to those in the 10 min ischemia-group. Our fining indicates that neuronal death/damage and gliosis of astrocytes and microglia were apparently increased with longer time of ischemia–reperfusion.
ARD1 is present in various species and has several variants derived from alternative splicing of mRNA. Previously, we reported differential biological functions and cellular distributions of mouse ...ARD1 (mARD1) variants. However, in comparison to mARD1 variants, human ARD1 (hARD1) variants have been rarely studied. In this study, we characterized a hARD1 variant, hARD1(131) and investigated its cellular activities. hARD1(131) mRNA was isolated from HeLa cells and sequenced. Sequence alignment revealed that, compared to hARD1(235), the most common form of hARD1, the mRNA sequence encoding hARD1131 possesses an altered reading frame due to a 46-bp deletion. Thus, hARD1(131) and hARD1(235) differ in their C-terminal regions with a partially deleted acetyltransferase domain at the C-terminus of hARD1(131). Moreover, hARD1(131) and hARD1(235) showed different subcellular localizations and biological functions. hARD1(131) was mostly localized in the cell nucleus, whereas hARD1(235) was primarily localized in the cytoplasm. In addition, hARD1(235) stimulated cell proliferation by upregulation of cyclin D1, however hARD1(131) had no influence on cyclin D1 expression and cell growth. Because hARD1(235) enhances cell proliferation by its autoacetylation activity, we examined the autoacetylation activity of hARD1(131) and observed that this function was absent in hARD1(131). These results suggest that human ARD1 variants have different effects on cell prolifer-ation, which may result from distinct subcellular localizations and autoacetylation activities.
Abstract Young animals appear much less vulnerable to ischemic insults. In present study, we compared neuronal damage and changes in the immunoreactivities and levels of inflammatory cytokine, ...interleukin (IL-) 2 as a pro-inflammatory cytokine and its receptor (IL-2Rβ), IL-4 and IL-13 as anti-inflammatory cytokines, in the hippocampal CA1 region between adult and young gerbils after 5 min of transient cerebral ischemia. Most (about 89%) of hippocampal CA1 pyramidal neurons showed neuronal damage only in the adult gerbil at 4 days post-ischemia; in the young ischemia-group, about 61% of CA1 pyramidal neurons showed neuronal damage at 7 days post-ischemia. Thereafter, the neuronal damage in the CA1 pyramidal neurons was not significantly changed in both the groups. IL-2 and IL-2Rβ immunoreactivity in the stratum pyramidale (SP) of the CA1 region was similar in both the sham groups. At 4 days post-ischemia, IL-2 and IL-2Rβ immunoreactivity in the adult SP was dramatically decreased; however, in the young SP, they were not changed, and they were decreased at 7 days post-ischemia. IL-4 and IL-13 immunoreactivity in the SP of the young sham-group were much lower than those in the adult group. Four days after ischemia-reperfusion, they were dramatically decreased in the adult ischemia-group; however, at this time, they were markedly increased in the young ischemia-group. In brief, our findings indicate that IL-2, 2Rβ, IL-4 and IL-13 immunoreactivity in young gerbils was similar or low compared to those in the adult, and they were decreased at 4 days post-ischemia in the adult; however, at this time, they were distinctively increased in the young.
Purpose The objective of this study was to examine the effect of step climbing exercise on the walking ability of stroke patients. Subjects and Methods Among hospitalized stroke patients, 24 were ...selected based on the study criteria and randomly divided into two groups: an experimental group (12 patients) and a control group (12 patients). The patients in both groups participated in 15-minute exercise sessions three times a week for eight weeks. To analyze the effect of the exercise, muscle strength, the Timed Up and Go test, and step length were measured before and after the exercise. Results step climbing exercise improved the muscle strength in the lower limbs of the stroke patients, as well as their Timed Up and Go results and step lengths. Conclusion The effects were similar to a stair gait exercise, and thus, step climbing may be more broadly applied to the treatment of stroke patients.
Purpose The objective of this study was to examine the effect of ankle strategy exercises on unstable surfaces on balance and walking ability in stroke patients. Subjects and Methods Among ...hospitalized stroke patients, 30 were selected based on the study criteria and were randomly divided into three groups: an ankle strategy group (n=10), balance exercise group (n=10), and control group (n=10). Patients in two groups (ankle strategy, balance exercise group) performed 15-minute exercise sessions three times a week for six weeks. To analyze the effect of the exercise, center of pressure, Berg balance Scale, Timed Up and Go test, and Functional Reach Test were assessed before and after the exercise. Results The ankle strategy exercise group showed more improvement in mediolateral center of pressure and Berg Balance Scale and Timed Up and Go test scores than the balance exercise group. Conclusion The results of this study suggest that ankle strategy exercises on unstable surfaces is feasible and efficacious for stroke patients.
Highlights ► We estimated the effectiveness of the influenza vaccine at preventing hospitalization. ► The overall vaccine effectiveness for preventing hospitalization was 32.5%. ► The effectiveness ...in patients aged ≥65 years with chronic heart disease was 72.6%.
Abstract Cytotoxic T lymphocyte antigen-4 (CTLA4) and IgG fusion protein, CTLA4-Ig, is a therapeutic agent used for rheumatoid arthritis. It binds B7 molecules on dendritic cells (DCs) and thereby ...blocks B7/CD28 costimulatory interaction and inhibits effective T cell proliferation. However, the effect of CTLA4-Ig on the regulatory T cell (Treg) is still not known. In this study, we investigated the influence of CTLA4-Ig on the CD4+CD25+Foxp3+ Treg population in collagen-induced arthritis (CIA) mouse model. CTLA4-Ig suppressed CIA and increased the CD4+CD25+Foxp3+ Treg population in joint and spleen. When CD11c + DCs and CD4+T cells from CIA mice were cultured with anti-CD3, CTLA4-Ig increased the CD4+CD25 + Foxp3+ Treg population in a TGF-β-dependent manner. When CD11c + DCs from CIA mice were treated with CTLA4-Ig and adoptively transferred into CIA-induced mice, arthritis did not develop in association with the increase in CD4+CD25+Foxp3+ Treg population. However, in CTLA4-Ig-untreated DC-transferred CIA mice, arthritis developed and then rapidly progressed. Our study demonstrated that CTLA4-Ig suppressed CIA by modifying DCs from CIA mice into tolerogenic DCs to increase the CD4+CD25+Foxp3+ Treg population and this seems to be the new immune regulatory mechanism of CTLA4-Ig.
PDF
